Various conditions can damage the myocardium and, in turn, such damage can alter electrical conduction of intrinsic and artificial myocardial stimuli. For example, ischemia can cause myocardial scarring that slows electrical conduction of a pacing stimulus or myocardial depolarization responsive to a pacing stimulus. Hence, after ischemia, a scar may delay depolarization of the myocardium responsive to a pacing stimulus. Ischemia and scaring can also lead to ventricular arrhythmias. For example, many ischemic cardiomyopathy patients experience left ventricle arrhythmias caused by altered zones of electrical conduction associated with injured tissue.
Anti-tachycardia pacing (ATP) has been utilized successfully to terminate ventricular arrhythmias in a great number of patients with ventricular tachycardia. ATP therapies work by disrupting wavefronts as they enter or exit these zones of altered conduction. An article by Schwab et al., “Right ventricular versus biventricular antitachycardia pacing in the termination of ventricular tachyarrhythmia in patients receiving cardiac resynchronization therapy” (J Cardiovasc Electrophysiol, Vol. 17, pp. 504-507, May 2006) proposed a study to assess differences between patients having implanted cardiac resynchronization therapy and defibrillation devices (CRT-D devices) programmed for right ventricular pacing and ATP or biventricular pacing and ATP. Some results for this study were reported by Gasparini (“Biventricular vs right ventricular antitachycardia pacing in the termination of ventricular tachyarrhythmia in patients receiving cardiac resynchronization therapy: The ADVANCE CRT-D trial. Heart Rhythm Society 2008 Scientific Sessions; May 15, 2008; San Francisco, Calif.). In a report of the results, it was stated (i) that arrhythmia symptoms (syncope or presyncope) during ATP of fast VT were more likely to develop with RV pacing, (ii) that “fast” VT might respond better to biventricular pacing while RV pacing may sometimes be best for slower VT episodes and (iii) that ATP with biventricular pacing appeared to be more effective in ischemic heart disease, with RV pacing performing better in nonischemic than ischemic patients (see, Stiles, “Antitach-pacing in CRT-treated heart failure explored in randomized study”, HRS News, Jun. 6, 2008). These results demonstrate that risk of, and termination of, arrhythmias with respect to pacing regimen are only understood superficially.
As described herein, various exemplary techniques aim to treat arrhythmias by delivering stimulation energy via different stimulation sites. Such techniques may be applied to pacing regimens that rely on biventricular pacing (e.g., as implemented by CRT or CRT-D devices) or other pacing regimens that can delivery energy via two or more sites.